scholarly journals Vaccination with Recombinant Baculovirus Expressing Ranavirus Major Capsid Protein Induces Protective Immunity in Chinese Giant Salamander, Andrias davidianus

Viruses ◽  
2017 ◽  
Vol 9 (8) ◽  
pp. 195 ◽  
Author(s):  
Xiaoyuan Zhou ◽  
Xinglang Zhang ◽  
Yahui Han ◽  
Qiuhong Jia ◽  
Hongwei Gao
2020 ◽  
Vol 47 (4) ◽  
pp. 2835-2843
Author(s):  
Ikbel Hadj Hassine ◽  
Jawhar Gharbi ◽  
Bechr Hamrita ◽  
Mohammed A. Almalki ◽  
José Francisco Rodríguez ◽  
...  

Viruses ◽  
2018 ◽  
Vol 10 (2) ◽  
pp. 52 ◽  
Author(s):  
Zhong-Yuan Chen ◽  
Tao Li ◽  
Xiao-Chan Gao ◽  
Chen-Fei Wang ◽  
Qi-Ya Zhang

Viruses ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 2224
Author(s):  
Yiqun Li ◽  
Yuding Fan ◽  
Yong Zhou ◽  
Nan Jiang ◽  
Mingyang Xue ◽  
...  

Chinese giant salamander iridovirus (GSIV) infection could lead to mitochondrial apoptosis in this animal, a process that involves B-cell lymphoma-2 (BCL-2) superfamily molecules. The mRNA expression level of Bcl-xL, a crucial antiapoptotic molecule in the BCL-2 family, was reduced in early infection and increased in late infection. However, the molecular mechanism remains unknown. In this study, the function and regulatory mechanisms of Chinese giant salamander (Andrias davidianus) Bcl-xL (AdBcl-xL) during GSIV infection were investigated. Western blotting assays revealed that the level of Bcl-xL protein was downregulated markedly as the infection progressed. Plasmids expressing AdBcl-xL or AdBcl-xL short interfering RNAs were separately constructed and transfected into Chinese giant salamander muscle cells. Confocal microscopy showed that overexpressed AdBcl-xL was translocated to the mitochondria after infection with GSIV. Additionally, flow cytometry analysis demonstrated that apoptotic progress was reduced in both AdBcl-xL-overexpressing cells compared with those in the control, while apoptotic progress was enhanced in cells silenced for AdBcl-xL. A lower number of copies of virus major capsid protein genes and a reduced protein synthesis were confirmed in AdBcl-xL-overexpressing cells. Moreover, AdBcl-xL could bind directly to the proapoptotic molecule AdBak with or without GSIV infection. In addition, the p53 level was inhibited and the mRNA expression levels of crucial regulatory molecules in the p53 pathway were regulated in AdBcl-xL-overexpressing cells during GSIV infection. These results suggest that AdBcl-xL plays negative roles in GSIV-induced mitochondrial apoptosis and virus replication by binding to AdBak and inhibiting p53 activation.


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